1. Field of the Invention
This invention relates generally to an system and method for providing pseudospontaneous neural stimulation. In particular, the invention relates to an apparatus and method for providing pseudospontaneous activity in the auditory nerve, which can be used to treat a sensorineural deafness patient. Electrical signals that induce pseudospontaneous neural activity in the auditory nerve can be delivered to the patient via an inner ear (cochlear) implant.
2. Background of the Related Art
At least two distinct types of hearing problems are recognized: conductive hearing loss and sensorineural hearing loss. The former is generally due to a mechanical defect in the middle ear that prevents sound-related vibrations from reaching the inner ear. In the latter, sound-related vibrations reach the inner ear, but signal transmission to the brain does not occur or is restricted. Sensorineural hearing loss usually results from damage to the cochlea and/or the auditory nerve. Sensorineural hearing loss is a common condition that may occur in old age, or may be due to exposure to excessively loud noises (e.g. rock concerts, jet engines), viral infections, etc.
Patients experiencing a certain amount of hearing loss may benefit from the use of a hearing aid which increases the volume of sound electronically, and which may be placed either behind the pinna of the ear or within the outer ear canal. In both cases, the device usually comprises a microphone for transforming sound waves into electrical signals, an amplifier for increasing the strength of the electrical signals, and an earphone for providing amplified sounds. Devices designed to treat deafness must obviously consider the underlying cause of deafness. For example, a sensorineural deafness patient with a defective cochlea who still has a functional auditory nerve, may benefit from a cochlear implant, as described hereinbelow. However, if the auditory nerve is itself damaged and cannot carry electrical signals, then the problem is “too far downstream” in the signal processing sequence for a cochlear implant to be effective. In that situation, artificial signals must enter the auditory system “beyond the block” for example, in the brain stem or in the auditory cortex.
Cochlear implants were designed for patients who are deaf as a result of loss of the cochlea's sound transduction mechanism. In this situation, an electrode is implanted in the cochlea whereby the electrode, upon receiving electrical signals from a speech processor directly stimulates the auditory nerve. Consequently, candidates for a cochlear implant device must have an intact auditory nerve capable of carrying electrical signals to the brain stem. The cochlear implant device delivers electrical signals e.g., by means of a multi-contact stimulating electrode. The stimulating electrode is surgically inserted by an otolaryngologist into the damaged cochlea. Activation of the contacts stimulates auditory nerve terminals that are normally activated by the cochlear sound transduction mechanism (hair cells-spiral ganglion). The patient perceives sound as the coded electrical signal carried into the brain by the auditory nerve. (See for example, Cohen, N. L. et al., “A Prospective, Randomized Study of Cochlear Implants,” N. Engl. J. Med., 328:233-7, 1993.)
Cochlear implants are surgically placed in the cochlea within the temporal bone with little risk to the patient, because patients who are already deaf due to a defective cochlea have little chance of any additional injury being caused by placement of a cochlear implant. In patients with hearing loss caused by dysfunction at the level of the cochlea, cochlear implants can restore hearing.
However, fundamental differences currently exist between electrical stimulation and acoustic stimulation of the auditory nerve. Electrical stimulation of the auditory nerve, for example, via a cochlear implant, generally results in more cross-fiber synchrony, less within fiber jitter, and less dynamic range, as compared with acoustic stimulation which occurs in individuals having normal hearing. As a result, hearing percepts experienced by sensorineural deafness patients via a cochlear implant lack the coherence and clarity characteristics of normal hearing.
FIG. 15 shows a related art pattern of electrically-evoked compound action potentials (EAPs) magnitudes from an auditory nerve of a human subject with an electrical stimulus of 1 kHz (1016 pulses/s). The EAP magnitudes are normalized to the magnitude of the first EAP in the record. FIG. 15 shows the typical alternating pattern previously described in the art. This pattern arises because of the refractory period of the nerve and can degrade the neural representation of the stimulus envelope. With a first stimulus 1502, a large response occurs likely because of synchronous activation of a large number of nerve fibers. These fibers are subsequently refractory during a second pulse 1504, and accordingly, a small response is generated. By the time of a third pulse 1506, an increased pool of fibers becomes available and the corresponding response increases. The alternating synchronized response pattern can be caused by a lack or decrease of spontaneous activity in the auditory nerve and can continue indefinitely.
The above reference is incorporated by reference herein where appropriate for appropriate teachings of additional or alternative details, features and/or technical background.